Zhizi Jing

Publications (2)13.64 Total impact

• Article: Chromosome 1 open reading frame 190 promotes activation of NF-κB canonical pathway and resistance of dendritic cells to tumor-associated inhibition in vitro.

  Zhizi Jing, Xin Yuan, Jing Zhang, Xin Huang, Zhiqian Zhang, Jingyi Liu, Miaomiao Zhang, Jiangbo Oyang, Yuan Zhang, Zhujun Zhang, Rongcun Yang
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  ABSTRACT: Tumor-associated dendritic cells (DCs) often induce T cell anergy or deletion and regulatory T cells instead of antitumor immunity. Although many tumor-associated Ags have been found, there is still no effective vaccine for cancer. Thus, novel rational strategies to enhance the immunogenicity of cancer-specific Ags are needed. Chromosome 1 open reading frame 190 (c1orf190), a gene that encodes a 239-aa hypothetical protein and contains multiple kinase phosphorylation sites, has a wide relationship with multiple signaling pathway molecules and can be regulated by multiple factors, such as TLR ligands. In this study, we demonstrate that c1orf190 can activate NF-κB, drive the production of cytokines, and promote the Ag-presenting function and the priming ability of DCs. Furthermore, c1orf190 can promote resistance of DCs to tumor-associated inhibition not only in the Ag-presenting function but also in the priming ability to induce Ag-specific T lymphocytes. Thus, c1orf190, an NF-κB activator, may be a candidate gene for regulating the function of DCs to resist tumor-associated factor-mediated dysfunction. We also found that c1orf190-mediated cytokine release is achieved by activating the canonical but not the noncanonical NF-κB pathway.
  The Journal of Immunology 11/2010; 185(11):6719-27. · 5.79 Impact Factor
• Article: Suppressor of cytokine signaling 3 promotes bone marrow cells to differentiate into CD8+ T lymphocytes in lung tissue via up-regulating Notch1 expression.

  Zhuohan Zhang, Bin Zeng, Zhiqian Zhang, Guohui Jiao, Haijie Li, Zhizi Jing, Jiangbo Ouyang, Xin Yuan, Limin Chai, Yongzhe Che, Yuan Zhang, Rongcun Yang
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  ABSTRACT: Suppressor of cytokine signaling 3 (SOCS3) expression in bone marrow cells (BMC) was up-regulated upon exposure to interleukin 6, lipopolysaccharide, or tumor-associated factors. But, how the up-regulated SOCS3 affects differentiation of BMCs is incompletely characterized. Here, we showed that SOCS3 promoted BMCs to intently differentiate into CD8 T cells. Importantly, lung can be as one athymus tissue for the BMCs to differentiate into CD8(+) T cells. Notch1 plays a critical role in the differentiation from SOCS3-transfected BMCs to CD8(+) T cells. We conclude that the up-regulated SOCS3 in some pathologic conditions, such as tumor and inflammation, might promote BMCs to differentiate into CD8(+) T lymphocytes in lung tissue via up-regulating Notch1 expression. This may represent a new mechanism against diseases such as tumor.
  Cancer Research 03/2009; 69(4):1578-86. · 7.86 Impact Factor